Investigating the mechanisms of hyporesponse to antiplatelet approaches

Eugene Braunwald, Dominick Angiolillo, Eric Bates, Peter B. Berger, Deepak Bhatt, Christopher P. Cannon, Mark I. Furman, Paul Gurbel, Alan D. Michelson, Eric Peterson, Stephen Wiviott

Research output: Contribution to journalArticlepeer-review

8 Scopus citations


Hyporesponsiveness, or resistance, to antiplatelet therapy may be a major contributor to poorer outcomes among cardiac patients and may be attributed to an array of mechanisms - both modifiable and unmodifiable. Recent evidence has uncovered clinical, cellular, and genetic factors associated with hyporesponsiveness. Patients with severe acute coronary syndromes (ACS), type 2 diabetes, and increased body mass index appear to be the most at risk for hyporesponsiveness. Addressing modifiable mechanisms may offset hyporesponsiveness, while recognizing unmodifiable mechanisms, such as genetic polymorphisms and diseases that affect response to antiplatelet therapy, may help identify patients who are more likely to be hyporesponsive. Hyporesponsive patients might benefit from different dosing strategies or additional antiplatelet therapies. Trials correlating platelet function test results to clinical outcomes are required. Results from these studies could cause a paradigm shift toward individualized antiplatelet therapy, improving predictability of platelet inhibition, and diminishing the likelihood for hyporesponsiveness.

Original languageEnglish (US)
Pages (from-to)I21-I27
JournalClinical Cardiology
Issue number3 SUUPL. 1
StatePublished - Mar 2008
Externally publishedYes


  • Acute coronary syndromes<ischemic heart disease
  • Catheterization/diagnostic interventional<cardiac
  • Myocardial infarction<ischemic heart disease
  • Platelets
  • Thrombosis/hypercoagulable states

ASJC Scopus subject areas

  • Cardiology and Cardiovascular Medicine


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